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    * Sarin *

    سارین


    Iranian_Flag_Hand_Love_Heart.jpg
    (Wikipedia) - Sarin For other uses, see Sarin (disambiguation). Not to be confused with Serine, Sarrin, or Saran (disambiguation). Sarin Identifiers Properties Hazards
    Preferred IUPAC name

    (RS)-Propan-2-yl methylphosphonofluoridate

    Other names

    (RS)-O-Isopropyl methylphosphonofluoridate; IMPF; GB; 2-(Fluoro-methylphosphoryl)oxypropane; Phosphonofluoridic acid, P-methyl-, 1-methylethyl ester

    CAS number 107-44-8 Y
    PubChem 7871
    ChemSpider 7583 Y
    UNII B4XG72QGFM N
    ChEBI CHEBI:75701 N
    ChEMBL CHEMBL509554 Y
    Jmol-3D images Image 1
    SMILES
    • FP(=O)(OC(C)C)C

    InChI
    • InChI=1S/C4H10FO2P/c1-4(2)7-8(3,5)6/h4H,1-3H3 Y Key: DYAHQFWOVKZOOW-UHFFFAOYSA-N Y

      InChI=1/C4H10FO2P/c1-4(2)7-8(3,5)6/h4H,1-3H3

      InChI=1/C4H10FO2P/c1-4(2)7-8(3,5)6/h4H,1-3H3 Key: DYAHQFWOVKZOOW-UHFFFAOYAY

    Molecular formula C4H10FO2P
    Molar mass 140.09 g mol−1
    Appearance Clear colorless liquid
    Odor Odorless in pure form
    Density 1.0887 g/cm³ (25 °C) 1.102 g/cm³ (20 °C)
    Melting point −56 °C (−69 °F; 217 K)
    Boiling point 158 °C (316 °F; 431 K)
    Solubility in water Miscible
    MSDS Lethal Nerve Agent Sarin (GB)
    EU classification Extremely Toxic (T+)
    Main hazards It is a lethal cholinergic agent.
    NFPA 704 1 4 0
    LD50 550 ug/kg (rat, oral)
    Except where noted otherwise, data are given for materials in their standard state (at 25 °C (77 °F), 100 kPa)
     N (verify) (what is: Y/N?)
    Infobox references

    Sarin, or GB, is an organophosphorus compound with the formula CH3P(O)F. It is a colorless, odorless liquid, used as a chemical weapon owing to its extreme potency as a nerve agent. It has been classified as a weapon of mass destruction in UN Resolution 687. Production and stockpiling of sarin was outlawed by the Chemical Weapons Convention of 1993, and it is classified as a Schedule 1 substance.

    Sarin can be lethal even at very low concentrations, with death following within 1 to 10 minutes after direct inhalation due to suffocation from lung muscle paralysis, unless some antidotes, typically atropine or biperiden and pralidoxime, are quickly administered to a person. People who absorb a non-lethal dose, but do not receive immediate medical treatment, may suffer permanent neurological damage.

    Contents

    Production and structure

    Sarin is a chiral molecule because it has four chemically distinct substituents attached to the tetrahedral phosphorus center. The SP form (the (–) optical isomer) is the more active enantiomer due to its greater binding affinity to acetylcholinesterase. The P-F bond is easily broken by nucleophilic agents, such as water and hydroxide. At high pH, sarin decomposes rapidly to nontoxic phosphonic acid derivatives. It is usually manufactured and weaponized as a racemic mixture—an equal mixture of both enantiomeric forms—by the alcoholysis reaction of methylphosphonyl difluoride with isopropyl alcohol:    Isopropylamine is also included in the reaction to neutralize the hydrogen fluoride byproduct. As a binary chemical weapon, it can be generated in situ by this same reaction.

    A by-product of sarin production is diisopropyl methylphosphonate (DIMP), which degrades into isopropyl methylphosphonic acid (IMPA).

    Biological effectsSarin (red), acetylcholinesterase (yellow), acetylcholine (blue)

    Like other nerve agents, sarin attacks the nervous system by interfering with the re-absorption of neurotransmitters at neuromuscular junctions. Death will usually occur as a result of asphyxia due to the inability to control the muscles involved in breathing function.

    Specifically, sarin is a potent inhibitor of acetylcholinesterase, an enzyme that degrades the neurotransmitter acetylcholine after it is released into the synaptic cleft. In vertebrates, acetylcholine is the neurotransmitter used at the neuromuscular junction, where signals are transmitted between neurons from the central nervous systems to muscle fibres. Normally, acetylcholine is released from the neuron to stimulate the muscle, after which it is degraded by acetylcholinesterase, allowing the muscle to relax. A build-up of acetylcholine in the synaptic cleft, due to the inhibition of cholinesterase, means the neurotransmitter continues to act on the muscle fibre, so that any nerve impulses are effectively continually transmitted.

    Sarin acts on cholinesterase by forming a covalent bond with the particular serine residue at the active site. Fluoride is the leaving group, and the resulting phosphoester is robust and biologically inactive.

    Its mechanism of action resembles that of some commonly used insecticides, such as malathion. In terms of biological activity, it resembles carbamate insecticides, such as Sevin, and the medicines pyridostigmine, neostigmine, and physostigmine.

    Degradation and shelf lifeRabbit used to check for leaks at sarin production plant, Rocky Mountain Arsenal (1970)

    The most important chemical reactions of phosphoryl halides is the hydrolysis of the bond between phosphorus and the fluoride. This P-F bond is easily broken by nucleophilic agents, such as water and hydroxide. At high pH, sarin decomposes rapidly to nontoxic phosphonic acid derivatives. The initial breakdown of sarin is into isopropyl methylphosphonic acid (IMPA), a chemical that is not commonly found in nature except as a breakdown product of sarin. IMPA then degrades into methylphosphonic acid (MPA), which can also be produced by other organophosphates.

    Sarin degrades after a period of several weeks to several months. The shelf life can be shortened by impurities in precursor materials. According to the CIA, some Iraqi sarin had a shelf life of only a few weeks, owing mostly to impure precursors.

    Its otherwise-short shelf life can be extended by increasing the purity of the precursor and intermediates and incorporating stabilizers such as tributylamine. In some formulations, tributylamine is replaced by diisopropylcarbodiimide (DIC), allowing sarin to be stored in aluminium casings. In binary chemical weapons, the two precursors are stored separately in the same shell and mixed to form the agent immediately before or when the shell is in flight. This approach has the dual benefit of solving the stability issue and increasing the safety of sarin munitions.

    Effects and treatment

    Sarin has a high volatility (ease with which a liquid can turn into a gas) relative to similar nerve agents, therefore inhalation can be very dangerous and even vapor concentrations may immediately penetrate the skin. A person’s clothing can release sarin for about 30 minutes after it has come in contact with sarin gas, which can lead to exposure of other people. People who absorb a non-lethal dose but do not receive immediate appropriate medical treatment may suffer permanent neurological damage.

    Even at very low concentrations, sarin can be fatal. Death may follow in 1 to 10 minutes after direct inhalation of a lethal dose unless antidotes, typically atropine and pralidoxime, are quickly administered. Atropine, an antagonist to muscarinic acetylcholine receptors, is given to treat the physiological symptoms of poisoning. Since muscular response to acetylcholine is mediated through nicotinic acetylcholine receptors, atropine does not counteract the muscular symptoms. Pralidoxime can regenerate cholinesterases if administered within approximately five hours. Biperiden, a synthetic acetylcholine antagonist, has been suggested as an alternative to atropine due to its better blood–brain barrier penetration and higher efficacy.

    Sarin is 26 times more deadly than cyanide. The LD50 of subcutaneously injected sarin in mice is 172 μg/kg. Treatment measures have been described.

    Initial symptoms following exposure to sarin are a runny nose, tightness in the chest and constriction of the pupils. Soon after, the victim has difficulty breathing and experiences nausea and drooling. As the victim continues to lose control of bodily functions, the victim vomits, defecates and urinates. This phase is followed by twitching and jerking. Ultimately, the victim becomes comatose and suffocates in a series of convulsive spasms. Moreover, common mnemonics for the symptomatology of organophosphate poisoning, including sarin gas, are the "killer B''s" of bronchorrhea and bronchospasm because they are the leading cause of death, and SLUDGE - Salivation, Lacrimation, Urination, Defecation, Gastrointestinal distress, and Emesis.

    Diagnostic tests

    Controlled studies in healthy men have shown that a nontoxic 0.43 mg oral dose administered in several portions over a 3 day interval caused average maximum depressions of 22 and 30%, respectively, in plasma and erythrocyte cholinesterase levels. A single acute 0.5 mg dose caused mild symptoms of intoxication and an average reduction of 38% in both measures of cholinesterase activity. Sarin in blood is rapidly degraded either in vivo or in vitro. Its primary inactive metabolites have in vivo serum half-lives of approximately 24 hours. The serum level of unbound isopropylmethylphosphonic acid (IMPA), a sarin hydrolysis product, ranged from 2-135 µg/L in survivors of a terrorist attack during the first 4 hours post-exposure. Sarin or its metabolites may be determined in blood or urine by gas or liquid chromatography, while cholinesterase activity is usually measured by enzymatic methods.

    History

    Sarin was discovered in 1938 in Wuppertal-Elberfeld in Germany by scientists at IG Farben attempting to create stronger pesticides; it is the most toxic of the four G-Series nerve agents made by Germany. The compound, which followed the discovery of the nerve agent tabun, was named in honor of its discoverers: Schrader, Ambros, Gerhard Ritter, and Van der Linde.

    Use as a weapon

    In mid-1939, the formula for the agent was passed to the chemical warfare section of the German Army Weapons Office, which ordered that it be brought into mass production for wartime use. A number of pilot plants were built, and a high-production facility was under construction (but was not finished) by the end of World War II. Estimates for total sarin production by Nazi Germany range from 500 kg to 10 tons. Though sarin, tabun and soman were incorporated into artillery shells, Germany did not use nerve agents against Allied targets.

    U.S. Honest John missile warhead cutaway, showing M134 Sarin bomblets (c. 1960)

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